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Are all cone cells connected directly to the brain?

Are all cone cells connected directly to the brain?


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Coming from a computing science background, I noticed that cameras have orders of magnitude fewer wires than pixels. For example, the Raspberry Pi Camera v2 has 8 megapixels, but only 10 wires connecting it to the board. In human-made systems, it is preferred to time-multiplex pixels over few wires or, even better, already compress or encode image information on the camera.

I was wondering if the human optical system features something similar. Does the eye compress, encode or time-multiplex the image "pixels" it captures before sending the information to the brain? Or is each cone cell ("pixel") connected directly to the brain?

(In case the latter: Wow! The optical nerve must have a huge bandwidth.)


Are all cone cells connected directly to the brain?

No. Cones connect to ganglial cells.

Let's explore the numbers. Our eyes contain about 6 million cone cells, 90 million rods, and comparative handfuls of additional photosensitive cells (ipRGC's) that don't play a role in vision.

The optic nerve is a bundle of roughly 1 million fibers (perhaps up to about 1.7 million). So by just running the numbers, it doesn't fit.

I was wondering if the human optical system features something similar. Does the eye compress, encode or time-multiplex the image "pixels" it captures before sending the information to the brain?

Let's focus on photopic vision (color vision, which happens when lighting conditions are sufficient).

Our perception of color starts not with the cones, but with ganglial cells in the retina. This is different than how an RGB camera works; our brains don't process color in terms of "pure cone signals". Instead, color is processed in three channels; a "red-green" channel that measures the difference between L cones and M cones; a "yellow-blue" channel that adds input of L and M cones and subtracts out contributions from S, and a "brightness" channel that computes the sum of all cones. This is referred to as opponent processes. Maybe we can call this encoding.

In addition to this, there are ganglial cells in our retina that contribute to edge detection. These cells work similarly to ganglial cells that perform difference measurements for opponent processes, only they connect to the same cone types. Since ganglial cells connect locally, if there's a large difference between stimulation of two cones next to each other, it's an indication that there's an image of an edge of something projected onto that spot. If we can't distinguish individual cones, but these things can distinguish edges which to us are the more interesting property, maybe we can call this lossy compression.

Outside of this, a huge amount of our brain is devoted to visual perception. There are some really strange quirks about our eyes; most popular is the existence of the blind spot. Additionally, our 90 million rods are squeezed more into peripheral vision, leading to fuzzier imaging in photopic conditions the farther away we are from the fovea. Furthermore, chromatic aberration can be quite a pain, but L and M cone sensitivities are very close to each other. So where absolute sharpness matters, we have less S cones around; in fact, in our foveola, there's nothing but L and M cones. Our brain makes up for this, by stimulating us to move our eyes constantly and rapidly (saccades). As we do so, the visual cortex goes into overdrive, filling in that blind spot, crisping up that periphery a bit, painting in an illusory blue in our center vision, etc. Though this involves "moving the camera around", we could maybe call this a sophisticated, high level form of time multiplexing.

Much of this information is available from wikipedia articles, though you might need to know what to look for; so here's a starting guide:

  • Cone_cell for cone cell counts
  • Fovea_centralis for cone density in center in vision, with picture
  • Optic_nerve for count of optic nerve bundle fibers
  • Opponent_process for opponent process theory
  • Receptive_field contains discussion of edge detection

Sense of Smell

Sense of smell is one of the senses that is processed by our nervous system to let us know more about our surroundings, and about the things we consume to keep the body healthy and safe. The smell is a sense of the information coming through the nose.

The sensory organ comprises specialized cells and tissues that recognize odourants, transfers a signal, which is received by nerve endings of the olfactory nerve, and processed finally by the nervous system. The brain interprets the signal as smell (olfaction). Smell let us know about our surrounding and gives us instincts about what is safe or dangerous.

Content: Sense of smell

Definition: Sense of Smell

A sense of smell is one’s ability to perceive the odour of things in the surrounding through the nose. The sense of smell is also known as an olfactory sense that unable us to detect pleasant, unpleasantness, or odourless things. Our sense of smell is a chemosensory mechanism that works by detecting chemicals present in the air via the nose (sensory organ).

Chemicals inhaled along with the air will get evaporate onto the olfactory epithelium, after which the olfactory nerve contracts and triggers an electrical response. The signal then moves along the path of the olfactory tract to the olfactory bulb (processes signal concerning memory and emotion), and finally to the neocortex region of the brain, which interprets the kind of smell we perceived.

What is Smell?

Smell or odour can define as the odour molecules (mixtures of light and small molecules) that are filled within the air, which are released from the volatile materials. An odour comes out of the substances that release volatile chemicals (in low concentrations) into the air, which can be perceived as a sense of smell.

Your nose can judge different smells by the presence of smell receptors that can recognize odour molecules in the air. When your nose sniffs the air, the smell receptors get alert and send a signal to your brain. Our brain can recognize different smells at a time that is entering your nose.

Example: Different dishes contain different spices that can give off many odour molecules. Our brain can piece together all this information and let us know which kind of dish is being cooked.

How do things smell?

As we all know that few things smell, while others don’t. The reason is that the smell comes out of the substances that give off particles into the air. To perceive the smell, those particles need to pass through our sensory organ that is the nose. The particles or chemicals releases by the living and non-living materials are grouped into volatile and non-volatile chemicals.

The majority of the living things release volatile chemicals or particles that evaporate easily and give off a stronger smell. Oppositely, non-volatile objects often do smell, rarely smell, or none at all. Generally, Smell can be either pleasant or unpleasant.


Smell Detection

Olfactory receptors recognize the odourants or volatile chemicals mixed with the air. A single odorant molecule shows varying affinity to attach with the number of olfactory receptors, depending on their physio-chemical properties.

  1. Once the odourants enter through the nasal cavity, the olfactory receptors sense such chemicals.
  2. Then the odorants selectively bind to the olfactory receptor, which results in structural changes in it.
  3. A structural change will turn on the olfactory-type G protein.
  4. Then, the G protein activates the adenylyl cyclase enzyme, which turns ATP into cyclic AMP (cAMP).
  5. After that, cAMP unfolds the cyclic nucleotide-gated ion channels, which allows passage for the calcium and sodium ions to get into the cell.
  6. The entry of calcium and sodium ions cause depolarization of the olfactory receptor neuron and generates an electrical impulse up to the olfactory bulb that first processes the information signal, and transfers it to the forebrain that decides the kind of smell.

Therefore, in the process of olfaction, the chemical information of the odourants converts into electrical information, which can be easily interpreted by the brain. The pathway of chemical signals to the brain is also linked with the regions (amygdala and hippocampus) of emotion and memory.

The sense of smell can change how we feel or what we think. This is the reason, where some people have a good sense of smell, while others have no sense of smell (anosmia). Smell loss can have a big impact on our psychological wellbeing.


Scientists convert human skin cells directly into brain cells

By exposing skin cells to a particular combination of cell programming molecules, scientists managed to convert them into brain cells that behave like native cells.

Share on Pinterest Human skin cells (top) can be converted into medium spiny neurons (bottom) with exposure to the right combination of microRNAs and transcription factors, according to work by Andrew Yoo and colleagues.
Image credit: Yoo Lab

The study is unusual because, unlike many cell conversion techniques, the cells did not return to a stem cell stage first – they converted directly into brain cells – thus avoiding the risk of producing many other types of cells.

And the study is unique, because the team managed to reprogram the skin cells to become a particular type of brain cell instead of a range of brain cells.

Writing in the journal Neuron, researchers from Washington University School of Medicine in St. Louis (WUSTL), MO, report how they used a particular combination of microRNAs and transcription factors to reprogram the skin cells into a particular type of brain cell known as medium spiny neurons.

The medium spiny neurons they produced – which survived for at least 6 months after injection into the brains of mice – are important for controlling movement and are the main type affected in Huntington’s disease.

Huntington’s disease is an inherited genetic disease that causes involuntary movements and gradual decline of mental ability. Patients with the disease – which usually starts in middle age – can live for 20 years after symptoms begin, although these gradually get worse.

Senior author Dr. Andrew S. Yoo, assistant professor of developmental biology at WUSTL, says not only did the new cells survive in the mouse brain, but they also showed properties similar to native cells:

“ These cells are known to extend projections into certain brain regions. And we found the human transplanted cells also connected to these distant targets in the mouse brain. That’s a landmark point about this paper.”

Because they used adult human skin cells in the study – and not mouse cells or human cells at an earlier stage of development – the team believes the work shows the potential for using patients’ own cells in regenerative medicine. This is important because therapies can use readily available cells and also avoid the problem of immune rejection.

For their study, Dr. Yoo and colleagues cultured the skin cells in an environment that mimics that of brain cells. In previous work, they had already discovered that exposing skin cells to two small RNA molecules called miR-9 and miR-124 can turn them into different types of brain cell.

Although they are still trying to work out exactly what happens, the team believes the two small RNA molecules open up the tightly packed DNA inside cells that holds instructions for making brain cells, allowing the genes particular to their development and function to be switched on.

Having proved that exposure to these small RNA molecules converts skin cells into a mix of brain cells, the team began fine-tuning the chemical signals. They did this by adding molecules called transcription factors that they already knew were present in the part of the brain where medium spiny neurons are abundant.

Co-first author Matheus B. Victor, a graduate student in neuroscience, says they believe the small RNA molecules are “doing the heavy lifting,” and:

“ They are priming the skin cells to become neurons. The transcription factors we add then guide the skin cells to become a specific subtype, in this case medium spiny neurons. We think we could produce different types of neurons by switching out different transcription factors.”

The team also showed that when the skin cells are exposed to the transcription factors alone, without the small RNA molecules, the skin cells do not convert successfully.

The team also carried out extensive tests to show the new brain cells had the hallmarks of native medium spiny neurons. They expressed the right genes for their specific type and did not express genes for other types of neurons.

And, when transplanted into the brains of mice, the converted cells looked like native medium spiny neurons and behaved like them.

The team is now using skin cells from patients with Huntington’s disease and converting them into medium spiny neurons using their new approach. They also plan to inject the cells into mice with the disease.

The study was funded by various bodies, including the National Institutes of Health (NIH).


Contents

Opsins can be classified several ways, including function (vision, phototaxis, photoperiodism, etc.), type of chromophore (retinal, flavine, bilin), molecular structure (tertiary, quaternary), signal output (phosphorylation, reduction, oxidation), etc. [1]

There are two groups of protein termed opsins. [2] [3] Type I opsins are employed by prokaryotes and by some algae (as a component of channelrhodopsins) and fungi, [4] whereas animals use type II opsins. No opsins have been found outside these groups (for instance in plants, or placozoans). [2]

At one time it was thought that type I and type II were related because of structural and functional similarities. With the advent of genetic sequencing it became apparent that sequence identity was no greater than could be accounted for by random chance. However, in recent years new methods have been developed specific to deep phylogeny. As a result, several studies have found evidence of a possible phylogenetic relationship between the two. [5] [6] [7] However, this does not necessarily mean that the last common ancestor of type I and II opsins was itself an opsin, a light sensitive receptor: all animal opsins arose (by gene duplication and divergence) late in the history of the large G-protein coupled receptor (GPCR) gene family, which itself arose after the divergence of plants, fungi, choanflagellates and sponges from the earliest animals. The retinal chromophore is found solely in the opsin branch of this large gene family, meaning its occurrence elsewhere represents convergent evolution, not homology. Microbial rhodopsins are, by sequence, very different from any of the GPCR families. [8] According to one hypothesis, both type-I and type-II opsins belong to the transporter-opsin-G protein-coupled receptor (TOG) superfamily, a proposed clade that includes G protein-coupled receptor (GPCR), Ion-translocating microbial rhodopsin (MR), and seven others. [9]

Type I opsins (also known as microbial opsins) are seven-transmembrane-domain proteins. Most of them are ion channels or pumps instead of proper receptors and do not bind to a G protein. Type I opsins are found in all three domains of life: Archaea, Bacteria, and Eukaryota. In Eukaryota, type I opsins are found mainly in unicellular organisms such as green algae, and in fungi. In most complex multicellular eukaryotes, type I opsins have been replaced with other light-sensitive molecules such as cryptochrome and phytochrome in plants, and type II opsins in Metazoa (animals). [10]

Microbial opsins are often known by the rhodopsin form of the molecule, i.e., rhodopsin (in the broad sense) = opsin + chromophore. Among the many kinds of microbial opsins are the proton pumps bacteriorhodopsin (BR) and xanthorhodopsin (xR), the chloride pump halorhodopsin (HR) the photosensors sensory rhodopsin I (SRI) and sensory rhodopsin II (SRII), as well as proteorhodopsin (PR), Neurospora opsin I (NOPI), Chlamydomonas sensory rhodopsins A (CSRA), Chlamydomonas sensory rhodopsins B (CSRB), channelrhodopsin (ChR), and archaerhodopsin (Arch). [11]

Several type I opsins, such as proteo- and bacteriorhodopsin, are used by various bacterial groups to harvest energy from light to carry out metabolic processes using a non-chlorophyll-based pathway. Beside that, halorhodopsins of Halobacteria and channelrhodopsins of some algae, e.g. Volvox, serve them as light-gated ion channels, amongst others also for phototactic purposes. Sensory rhodopsins exist in Halobacteria that induce a phototactic response by interacting with transducer membrane-embedded proteins that have no relation to G proteins. [12]

Type I opsins (like channelrhodopsin, halorhodopsin, and archaerhodopsin) are used in optogenetics to switch on or off neuronal activity. Type I opsins are preferred if the neuronal activity should be modulated at higher frequency, because they respond faster than type II opsins. This is because type I opsins are ion channels or proton/ion pumps and thus are activated by light directly, while type II opsins activate G-proteins, which then activate effector enzymes that produce metabolites to open ion channels. [13]

Type II opsins (or animal opsins) are members of the seven-transmembrane-domain proteins (35–55 kDa) of the G protein-coupled receptor (GPCR) superfamily. [14]

Type II opsins fall phylogenetically into four groups: C-opsins (Ciliary), Cnidops (cnidarian opsins), R-opsins (rhabdomeric), and Go/RGR opsins (also known as RGR/Go or Group 4 opsins). The Go/RGR opsins are divided into four sub-clades: Go-opsins, RGR, Peropsins, and Neuropsins. C-opsins, R-opsins, and the Go/RGR opsins are found only in Bilateria. [15] [16]

Type II visual opsins are traditionally classified as either ciliary or rhabdomeric. Ciliary opsins, found in vertebrates and cnidarians, attach to ciliary structures such as rods and cones. Rhabdomeric opsins are attached to light-gathering organelles called rhabdomeres. This classification cuts across phylogenetic categories (clades) so that both the terms "ciliary" and "rhabdomeric" can be ambiguous. Here, "C-opsins (ciliary)" refers to a clade found exclusively in Bilateria and excludes cnidarian ciliary opsins such as those found in the box jellyfish. Similarly, "R-opsin (rhabdomeric)" includes melanopsin even though it does not occur on rhabdomeres in vertebrates. [15]

C-opsins (ciliary) Edit

Ciliary opsins (or c-opsins) are expressed in ciliary photoreceptor cells, and include the vertebrate visual opsins and encephalopsins. [17] They convert light signals to nerve impulses via cyclic nucleotide gated ion channels, which work by increasing the charge differential across the cell membrane (i.e. hyperpolarization. [2] )

Vertebrate visual opsins Edit

Vertebrate visual opsins are a subset of C-opsins (ciliary). They are expressed in the vertebrate retina and mediate vision. They can be further subdivided into rod opsins and four types of cone opsin. [17] Rod opsins (rhodopsins, usually denoted Rh), [18] are used in dim-light vision, are thermally stable, and are found in the rod photoreceptor cells. Cone opsins, employed in color vision, are less-stable opsins located in the cone photoreceptor cells. Cone opsins are further subdivided according to their absorption maxima (λmax), the wavelength at which the highest light absorption is observed. Evolutionary relationships, deduced using the amino acid sequence of the opsins, are also frequently used to categorize cone opsins into their respective group. Both methods predict four general cone opsin groups in addition to rhodopsin. [19]

Vertebrates typically have four cone opsins (LWS, SWS1, SWS2, and Rh2) inherited from the first vertebrate (and thus predating the first vertebrate), as well as the rod opsin, rhodopsin (Rh1), which emerged after the first vertebrate but before the first Gnathostome (jawed vertebrate). These five opsins emerged through a series of gene duplications beginning with LWS and ending with Rh1. Each one has since evolved into numerous variants and thus constitutes an opsin family or subtype. [20] [21]

Humans have the following set of photoreceptor proteins responsible for vision:

    (Rh1, OPN2, RHO) – expressed in rod cells, used in night vision
  • Three cone opsins (also known as photopsins) – expressed in cone cells, used in color vision
    • Long-wavelength sensitive (OPN1LW) Opsin – λmax of 560 nm, in the yellow-green region of the electromagnetic spectrum. [22] May be called the "red opsin," "erythrolabe," "L opsin" or "LWS opsin." Note that despite its common name as the "red" opsin, this opsin's peak sensitivity is not in the red region of the spectrum. However, it is more sensitive to red than the other two human opsins. [22] This receptor also has a secondary response in the violet high frequencies. [23][24]
    • Middle-wavelength sensitive (OPN1MW) Opsin – λmax of 530 nm, in the green region of the electromagnetic spectrum. [22] May be called the "green opsin," "chlorolabe," "M opsin" or "MWS opsin."
    • Short-wavelength sensitive (OPN1SW) Opsin – λmax of 430 nm, in the blue region of the electromagnetic spectrum. [22] May be called the "blue opsin," "cyanolabe," "S opsin" or "SWS opsin."

    Pinopsins Edit

    The first Pineal Opsin (Pinopsin) was found in the chicken pineal gland. It is a blue sensitive opsin (λmax = 470 nm). [25]

    wide range of expression in the brain, most notably in the pineal region

    Vertebrate Ancient (VA) opsin Edit

    Vertebrate Ancient (VA) opsin has three isoforms VA short (VAS), VA medium (VAM), and VA long (VAL). It is expressed in the inner retina, within the horizontal and amacrine cells, as well as the pineal organ and habenular region of the brain. [26] It is sensitive to approximately 500 nm [14], found in most vertebrate classes, but not in mammals. [27]

    Parapinopsins Edit

    The first parapinopsin (PP) opsin was found in the parapineal organ of the catfish. [28] The parapinopsin of lamprey is a UV-sensitive opsin (λmax = 370 nm). [29] The teleosts have two groups of parapinopsins, one is sensitive to UV (λmax = 360-370 nm), the other is sensitive to blue (λmax = 460-480 nm) light. [30]

    Parietopsins Edit

    The first parietopsin was found in the photoreceptor cells of the lizard parietal eye. The lizard parietopsin is green-sensitive (λmax = 522 nm), and despite it is a c-opsin, like the vertebrate visual opsins, it does not induce hyperpolarization via a Gt-protein, but induces depolarization via a Go-protein. [31] [32]

    OPN3 (Encephalopsin or Panopsin) Edit

    Panopsins are found in many tissues (skin, [33] brain, [34] [35] testes, [34] heart, liver, [35] kidney, skeletal muscle, lung, pancreas and retina [35] ). They were originally found in the human and mouse brain and thus called encephalopsin. [34]

    The first invertebrate panopsin was found in the ciliary photoreceptor cells of the annelid Platynereis dumerilii and is called c(iliary)-opsin. [36] This c-opsin is UV-sensitive (λmax = 383 nm) and can be tuned by 125 nm at a single amino-acid (range λmax = 377 - 502 nm). [37] Thus, not unsurprisingly, a second but cyan sensitive c-opsin (λmax = 490 nm) exists in Platynereis dumerilii. [38] The first c-opsin mediates in the larva UV induced gravitaxis. The gravitaxis forms with phototaxis a ratio-chromatic depth-gauge. [39] In different depths, the light in water is composed of different wavelengths: First the red (> 600 nm) and the UV and violet (< 420 nm) wavelengths disappear. The higher the depth the narrower the spectrum so that only cyan light (480 nm) is left. [40] Thus, the larvae can determine their depth by color. The color unlike brightness stays almost constant independent of time of day or the weather, for instance if it is cloudy. [41] [42]

    Panopsins are also expressed in the brains of some insects. [17] The panopsins of mosquito and pufferfish absorb maximally at 500 nm and 460 nm, respectively. Both activate in vitro Gi and Go proteins. [43]

    The panopsins of teleost fish are called: Teleost multiple tissue (TMT) opsins.

    Teleost Multiple Tissue (TMT) Opsin Edit

    Teleost fish opsins are expressed in many tissues and therefore called Teleost Multiple Tissue (TMT) opsins. [44] TMT opsins form three groups which are most closely related to a fourth groups the panopsins. [45] [46] In fact, TMT opsins in teleost fish are orthologous to the panopsins in the other vertebrates. They also have the same introns and the same place, which confirms that they belong together. [44]

    Cnidarian opsins Edit

    Cnidaria, which include jellyfish, corals, and sea anemones, are the most basal animals to possess complex eyes. Jellyfish opsins in the rhopalia couple to Gs-proteins raising the intracellular cAMP level. [47] [48] Coral opsins can couple to Gq-proteins and Gc-proteins. Gc-proteins are a subtype of G-proteins specific to cnidarians. [49] The cnidarian opsins have been identified as one group and so called cnidops, [15] however at least some of them belong to the c-opsins, r-opsins, and Go/RGR-opsins found in bilaterians. [14] [50] [51]

    R-opsins (rhabdomeric) / Gq-coupled Edit

    Rhabdomeric opsins (or r-opsins) are also known as Gq-opsins, because they couple to a Gq-protein. R-opsins are used by molluscs and arthropods. Arthropods appear to attain colour vision in a similar fashion to the vertebrates, by using three (or more) distinct groups of opsins, distinct both in terms of phylogeny and spectral sensitivity. [17] The r-opsin melanopsin is also expressed in vertebrates, where it regulates circadian rhythms and mediates the pupillary reflex. [17]

    Unlike c-opsins, r-opsins are associated with canonical transient receptor potential ion channels these lead to the electric potential difference across a cell membrane being eradicated (i.e. depolarization). [2]

    The identification of the crystal structure of squid rhodopsin [52] is likely to further our understanding of its function in this group.

    Arthropods use different opsins in their different eye types, but at least in Limulus the opsins expressed in the lateral and the compound eyes are 99% identical and presumably diverged recently. [53]

    Melanopsin OPN4 Edit

    Involved in circadian rhythms, pupillary reflex, and color correction in high-brightness situations. Phylogenetically a member of the R-opsin (rhabdomeric) group, functionally and structurally an r-opsin, but does not occur in rhabdomeres.

    Go/RGR (Group 4) opsins Edit

    Go/RGR opsins include Go-opsins, RGR-opsins, neuropsins, and peropsins.

    Go-opsins Edit

    Go-opsins are absent from higher vertebrates [15] and ecdysozoans. [54] They are found in the ciliary photoreceptor cells of the scallop eye [55] and the basal chordate amphioxus. [56] In Platynereis dumerilii however, a Go-opsin is expressed in the rhabdomeric photoreceptor cells of the eyes. [40]

    RGR opsins Edit

    RGR opsins, also known as Retinal G protein coupled receptors are expressed in the retinal pigment epithelium (RPE) and Müller cells. [57] They preferentially bind all-trans-retinal in the dark instead of 11-cis-retinal. [58] RGR opsins were thought to be photomerases [19] but instead, they regulate retinoid traffic and production. [17] [59] In particular, they speed up light-independently the production of 11-cis-retinol (a precursor of 11-cis-retinal) from all-trans-retinyl-esters. [60] However, the all-trans-retinyl-esters are made available light-dependently by RGR-opsins. Whether RGR-opsins regulate this via a G-protein or another signaling mechanism is unknown. [61] The cattle RGR opsin absorbs maximally at different wavelengths depending on the pH-value. At high pH it absorbs maximally blue (469 nm) light and at low pH it absorbs maximally UV (370 nm) light. [62]

    Peropsin Edit

    Peropsin, a visual pigment-like receptor, is a protein that in humans is encoded by the RRH gene. [63]

    Neuropsins Edit

    Neuropsins are sensitive to UVA, typically at 380 nm. They are found in the brain, testes, skin, and retina of humans and rodents, as well as in the brain and retina of birds. In birds and rodents they mediate ultraviolet vision. [33] [64] [65] They couple to Gi-proteins. [64] [65] In humans, Neuropsin is encoded by the OPN5 gene. In the human retina, its function is unknown. In the mouse, it photo-entrains the retina and cornea at least ex vivo. [66]

    Unclassified Edit

    Extraretinal (or extra-ocular) Rhodopsin-Like Opsins (Exo-Rh) Edit

    These pineal opsins, found in the Actinopterygii (ray-finned fish) apparently arose as a result of gene duplication from Rh1 (rhodopsin). These opsins appear to serve functions similar to those of pinopsin found in birds and reptiles. [67] [68]

    Opsin proteins covalently bind to a vitamin A-based retinaldehyde chromophore through a Schiff base linkage to a lysine residue in the seventh transmembrane alpha helix. In vertebrates, the chromophore is either 11-cis-retinal (A1) or 11-cis-3,4-didehydroretinal (A2) and is found in the retinal binding pocket of the opsin. The absorption of a photon of light results in the photoisomerization of the chromophore from the 11-cis to an all-trans conformation. The photoisomerization induces a conformational change in the opsin protein, causing the activation of the phototransduction cascade. The opsin remains insensitive to light in the trans form. It is regenerated by the replacement of the all-trans retinal by a newly synthesized 11-cis-retinal provided from the retinal epithelial cells. Opsins are functional while bound to either chromophore, with A2-bound opsin λmax being at a longer wavelength than A1-bound opsin.

    Opsins contain seven transmembrane α-helical domains connected by three extra-cellular and three cytoplasmic loops. Many amino acid residues, termed functionally conserved residues, are highly conserved between all opsin groups, indicative of important functional roles. All residue positions discussed henceforth are relative to the 348 amino acid bovine rhodopsin crystallized by Palczewski et al. [69] Lys296 is conserved in all known opsins and serves as the site for the Schiff base linkage with the chromophore. Cys138 and Cys110 form a highly conserved disulfide bridge. Glu113 serves as the counterion, stabilizing the protonation of the Schiff linkage between Lys296 and the chromophore. The Glu134-Arg135-Tyr136 is another highly conserved motif, involved in the propagation of the transduction signal once a photon has been absorbed.

    Certain amino acid residues, termed spectral tuning sites, have a strong effect on λmax values. Using site-directed mutagenesis, it is possible to selectively mutate these residues and investigate the resulting changes in light absorption properties of the opsin. It is important to differentiate spectral tuning sites, residues that affect the wavelength at which the opsin absorbs light, from functionally conserved sites, residues important for the proper functioning of the opsin. They are not mutually exclusive, but, for practical reasons, it is easier to investigate spectral tuning sites that do not affect opsin functionality. For a comprehensive review of spectral tuning sites see Yokoyama [70] and Deeb. [71] The impact of spectral tuning sites on λmax differs between different opsin groups and between opsin groups of different species.


    Are all cone cells connected directly to the brain? - Biology

    Brown researchers find new photoreceptor and visual system in the eye

    Rods and cones are not the only photoreceptors in our eyes. Reporting in the February 8 issue of Science, researchers at Brown University describe a third photoreceptor and a parallel visual system. The newly discovered cells turn light energy directly into brain signals. The signals govern the body’s 24-hour clock.

    PROVIDENCE, R.I. — Brown University researchers have found a new cell in the eye that acts as a photoreceptor – like a rod or cone – and sets the body’s circadian clock.

    For nearly 150 years, scientists considered rods and cones to be the eye’s only photoreceptors – cells that turn light energy into electrical impulses. Many cells in the eye and brain respond to light but only because they are linked to the rods and cones by complex pathways. These cells are responsible for the nervous system’s sensitivity to patterns, objects and movement in the visual world.

    Now there is a third photoreceptor, say scientists at Brown. The new cell resides deeper in the retina than rods and cones and looks remarkably different, more like the underside of a canopy of twisted tree branches.

    The scientists dub the new cell “an intrinsically photosensitive ganglion cell.” It also turns light energy directly into brain signals. These signals govern the body’s 24-hour clock, they say, adding that this retinal input is what helps people get over jet lag.

    In the February 8 issue of Science, the researchers describe the new cells, discovered in the retinas of rats, and their direct pipeline to the brain. The cells send out nerve fibers which travel within the optic nerve and connect with the clock region in the brain.

    “We think this population of cells plays a role in setting the circadian clock and probably in a variety of other functions where all the brain needs to know is how bright it is,” said lead author David Berson, associate professor of neuroscience. “It is a visual system that runs parallel to the one we have been thinking about all these years. Now we have to rethink how the retina works and how the brain understands what is going on in the visual world. This is a new kind of representation of light by the nervous system, a new way for the brain to react to the visual environment.”

    The scientists went looking for the cells in an effort to explain why some people who are functionally blind – whose rods and cones do not work – can still adjust their biological rhythms to match the day and night of the external world.

    “There is a strong likelihood that there are identical cells in humans,” Berson said. “This could explain why certain people who are functionally blind due to retinal degeneration continue to set their biological clock according to the day/night cycle. These people have suffered damage to photoreceptors and to a visual system we knew about. What we didn’t know until now was what sort of photoreceptor system still operated.”

    In experiments, the researchers injected a fluorescent dye into the tiny part of a rat’s brain that governs the 24-hour clock cycle. The dye traveled back to the new photoreceptors in the eye. The researchers then found the dye-filled cells, recorded their electrical activity, and found that they continued responding to light whether or not they were connected to the retina or brain.

    “We concluded that a response to light was intrinsic to these cells,” Berson said. Although scientists have long known that ganglion cells – the output cells of the retina – play a key role in vision, they were not considered to have any photoreceptors among them.

    A photoreceptor is a cell in the eye that contains a chemical called a photopigment that changes its properties in response to light. This change triggers a cascade of biochemical reactions and an electrical response in the photoreceptor. This signal then moves along a pathway between the cells and the brain.

    The paper’s coauthors include undergraduate Felice Dunn and postdoctoral researcher Motoharu Takao. The National Eye Institute funded the research.

    Berson and Takao are two of the co-authors of another paper in the February 8 issue of Science that points to the chemical melanopsin as the likely photopigment in these cells and traces their pathways to the brain. The other authors of that paper are from the Howard Hughes Medical Institute and Johns Hopkins University School of Medicine.

    Sights and Sounds of Science

    The newly discovered retinal photoreceptor, right, is an intrinsically photosensitive ganglion cell. The transduction of light into electrical signals appears to take place throughout the cell body (the dark, dyed circular structure) as well as in its slender, tangled dentrites.

    In this recording, the cell’s electrical activity has been transformed so the human ear can hear it. As the recording begins, the cell sits in the dark, awaiting a stimulus. About 10 seconds into the recording, a tone sounds, marking the moment when a bright light is turned on and kept on. For several seconds, there is no detectable response from the cell, but eventually it begins to fire nerve impulses, heard as popping sounds. The delay between the onset of stimulus and the beginning of the response is extraordinarily long compared with conventional photoreceptors (rods and cones). This is presumably because the newly discovered photoreceptors are specialized to detect slow changes in environmental lighting, not the rapid events that are so important in pattern vision. With constant light stimulation, the rate of firing gradually increases and then plateaus at a rate that encodes the intensity of the light flooding the cell.


    Inferior olive

    The olivo-cerebellar network provides the timing signals necessary for precise coordination of motor actions, and for non-motor and cognitive tasks. Within the network, neurons of the inferior olive (IO) provide the powerful excitatory climbing fiber input to Purkinje neurons. The clock of the timing signals in the cerebellum is thought to be provided by subthreshold 5–10 Hz oscillations produced by intrinsic mechanisms within neurons of the IO [37–39]. Electrical coupling between IO cells is thought to synchronize their sparse spikes [37, 40, 41].

    IO neurons are also influenced by GABAergic input from the cerebellar nuclei in IO glomeruli, where dendrites of neighboring IO neurons are connected via gap junctions [42] that are thus electrotonically distant from the somatic integrator. [For this reason, coupling coefficients measured between somas in IO neurons are typically weak [40]]. Rodolfo Llinás and colleagues hypothesized that electrical coupling between IO neurons is transiently modulated by synaptic inputs that act as a shunt between the GJs and soma, which results in an apparent depression of electrical synapse strength [43]. This mechanism has been recently directly confirmed by optogenetic activation of GABAergic input from the cerebellar nuclei that caused a transient decrease in electrical coupling strength between olivary cells [44].

    Another recent set of work has investigated long-term electrical synaptic plasticity coincident with glutamatergic activity in this structure. Long-term potentiation of electrical synapses between pairs of IO cells results from high-frequency stimulation or NMDA application, an effect dependent on intracellular Ca 2+ and CaMKII activity [45]. Conversely, lower-frequency stimulation (1 Hz) of adjacent white matter leads to depression of coupling, an effect also mediated via activation of NMDA receptors [46]. The involvement of NMDA receptors in triggering both activity-dependent potentiation and depression of synaptic transmission was previously reported for chemical synapses [47]. NMDAR-dependent bi-directional plasticity of electrical transmission in the IO is likely related to differences in the induction protocols or small variations in the experimental conditions.

    Coupling among IO neurons is highly variable, heterogeneity that was proposed to result from short-term activity-dependent plasticity at individual glomeruli [48]. Coupling was also reported to be asymmetrical [40], suggesting that substructures or microcircuits within IO circuits, defined by coupling, are formed and adjusted by ongoing changes in the strength of electrical synapses. Indeed, plasticity of electrical synapses has been proposed as a mechanism whereby motor learning and increased precision of timing is accomplished by gradual reduction of coupling strength in small subsets of IO neurons [49].


    Scientists see path for the coronavirus to invade the brain

    Scientists experimenting in the lab have found that the coronavirus that causes COVID-19 is capable of infecting two types of brain cells — neurons and astrocytes.

    The findings could shed light on a possible reason for the bewildering array of neurological symptoms that follow some COVID-19 survivors even after they recover.

    COVID-19 is best known as a respiratory disease, but for many victims, it also triggers an array of problems including memory lapses, fatigue and a certain sluggish, fuzzy feeling often referred to as “brain fog.”

    Scientists have been trying to understand why and how a coronavirus infection causes these issues in the brain, said study leader Diana Cruz-Topete, a molecular endocrinologist at Louisiana State University Health Shreveport.

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    Is the virus causing these problems indirectly — for example, by causing significant inflammation or clotting? Or is it causing them directly, by infecting cells in the brain?

    Theoretically, the latter would be a tricky proposition since it would depend on two things. The first is whether the SARS-CoV-2 virus can attack cells of the central nervous system. The second is whether the virus can gain access to the brain, which is protected by a semipermeable barrier that can block out pathogens and other harmful particles while still allowing nutrients and other key molecules to make it through.

    Cruz-Topete and her colleagues focused on the first issue. They examined cells typically found in the brain and spinal cord to see if they were vulnerable to infection.

    One-third of COVID-19 survivors were diagnosed with a psychiatric or neurological condition within six months of being infected with the coronavirus.

    The SARS-CoV-2 virus attacks human cells by targeting what are known as ACE2 receptors. These receptors are proteins that cover the surface of many types of cells, including those of the lungs, heart, kidneys and liver. But it’s been unclear whether cells in the brain and spinal cord even have the ACE2 receptors the coronavirus needs to mount an invasion.

    To find out, the researchers needed to know whether brain cells express ACE2 receptors and, if so, whether they can be infected.

    The scientists took human neural cells grown in laboratory dishes and studied the RNA and proteins they produced to look for evidence that ACE2 was being expressed. They examined neurons as well as astrocytes, supportive cells in the brain and spinal cord that outnumber neurons by more than 5 to 1.

    These star-shaped cells help maintain several key functions in the central nervous system and maintain the semipermeable boundary known as the blood-brain barrier. They also ferry nutrients from the bloodstream to neurons and prevent dangerous substances from getting in.

    “Astrocytes are cells that are in close contact with the blood-brain barrier,” Cruz-Topete said. If the virus were somehow to breach the barrier, astrocytes — if they were vulnerable to infection — would be among its most easily reached targets.

    Both astrocytes and neurons did express the ACE2 receptor, the scientists found. The next step was to see whether the brain cells could actually be infected.

    To do so, they used a surrogate virus modified to express the spike protein — the one that allows the coronavirus to “unlock” the ACE2 receptor and enter a cell. The engineered virus also expressed a green fluorescent protein that made it easy to spot after infecting a cell.

    The scientists unleashed their virus on both astrocytes and neurons and found that both types of brain cells can be infected with SARS-CoV-2. However, the astrocytes were significantly less likely than neurons to become infected.

    The researchers aren’t sure why that would be. Regardless of the reason, since there are so many of them, they provide the virus ample opportunity to invade and replicate.

    Once the astrocytes are infected, they could potentially be used as a steppingstone for the virus to reach more vulnerable neurons, the researchers said. That could explain many of the neurologic symptoms seen in COVID-19 patients, including loss of sense of smell and taste, disorientation, psychosis and stroke, the scientists said.

    The findings were presented last week at the American Physiological Society’s annual Experimental Biology meeting.

    The study has some limitations. For example, the experiments in the lab may not reflect what the virus does in the complex environment of a living body. A recent report in JAMA Psychiatry noted that SARS-CoV-2 viral particles have been found in brain vascular endothelium — the organ that makes up the blood-brain barrier — but not in neurons or astrocytes.

    Dr. Maura Boldrini, a psychiatrist and neuroscientist at Columbia University who was not involved in the research, said a big question remains: Even if brain cells are vulnerable to infection, how exactly could the virus cross the blood-brain barrier?

    “The main studies have shown that we don’t think there is a lot of penetration of the virus itself in the brain except in specific places,” said Boldrini, lead author of the JAMA Psychiatry paper.


    Are all cone cells connected directly to the brain? - Biology

    There are two types of photoreceptors in the human retina, rods and cones .

    Rods are responsible for vision at low light levels ( scotopic vision ). They do not mediate color vision, and have a low spatial acuity.

    Cones are active at higher light levels ( photopic vision ), are capable of color vision and are responsible for high spatial acuity. The central fovea is populated exclusively by cones. There are 3 types of cones which we will refer to as the short-wavelength sensitive cones, the middle-wavelength sensitive cones and the long-wavelength sensitive cones or S-cone, M-cones, and L-cones for short.

    The light levels where both are operational are called mesopic .

    The bottom figure shows the distribution of rods and cones in the retina. This data was prepared from histological sections made on human eyes.

    In the top figure, you can relate visual angle to the position on the retina in the eye.

    Notice that the fovea is rod-free and has a very high density of cones. The density of cones falls of rapidly to a constant level at about 10-15 degrees from the fovea. Notice the blind spot which has no receptors.

    At about 15°-20° from the fovea, the density of the rods reaches a maximum. (Remember where Hecht, Schlaer, and Pirenne presented their stimuli.) A longitudinal section would appear similar however there would be no blind spot. Remember this if you want to present peripheral stimuli and you want to avoid the blind spot.

    Here is a figure from the textbook that shows the changes in the size of the photoreceptors with eccentricity. The bottom graph shows individual variations in the density of cones.

    Here are schematic diagrams of the structure of the rods and cones:

    This figure shows the variety in the shapes and sizes of receptors across and within species.

    Here is a summary of the properties and the differences in properties between the rods and cones:

    If you look above at the schematic diagram of the rods and cones, you will see that in the outer segments of rods the cell membrane folds in and creates disks. In the cones, the folds remain making multiple layers. The photopigment molecules reside in membranes of these disks and folds. They are embedded in the membranes as shown in the diagram below where the two horizontal lines represent a rod disk membrane (either the membrane on the top or bottom of the disk) and the circles represent the chain of amino acids that make up a rhodopsin molecule. Rhodopsin is the photopigment in rods.

    Each amino acid, and the sequence of amino acids are encoded in the DNA. Each person possesses 23 pairs of chromosomes that encode the formation of proteins in sequences of DNA. The sequence for a particular protein is called a gene. In recent years, researchers have identified the location and chemical sequence of the genes that encode the photopigments in the rods and cones.

    This figure shows the structure of the rhodopsin molecule. The molecule forms 7 columns that are embedded in the disk membrane. Although not shown in this schematic, the columns are arranged in a circle like the planks of a barrel. (Another molecule called a chromophore binds within this barrel.)

    Each circle is an amino-acid which are the building blocks of proteins. Each amino acid is encoded by a sequence of three nucleic acids in the DNA.

    Before identifying the genetic sequence of human rhodopsin, it was sequences in other animals. Here is shown the comparison between the bovine (cow) sequence and the human sequence. They are very similar with only a small number of differences (the dark circles). Even when there is a difference it may not be functionally significant.

    The gene for human rhodopsin is located on chromosome 3.

    This figure shows the sequence for the S-cone pigment compared to that of rhodopsin. The S-cone pigment gene is located on chromosome 7. Notice how different they are.

    This figure shows the sequence of the L- and M-cone pigments compared to each other. These pigments are very similar. Only those differences within the cell membrane can contribute to the differences in their spectral sensitivity.

    The M- and L- cone pigments are both encoded on the X chromosome in tandem. The 23rd pair of chromosomes determines gender. For females this pair is XX and for males this pair is XY.

    We will return to this later on when we discuss color vision and color blindness.

    This figure shows how the three cone types are arranged in the fovea. Currently there is a great deal of research involving the determination of the ratios of cone types and their arrangement in the retina.

    This diagram was produced based on histological sections from a human eye to determine the density of the cones. The diagram represents an area of about 1° of visual angle. The number of S-cones was set to 7% based on estimates from previous studies. The L-cone:M-cone ratio was set to 1.5. This is a reasonable number considering that recent studies have shown wide ranges of cone ratios in people with normal color vision. In the central fovea an area of approximately 0.34° is S-cone free. The S-cones are semi-regularly distributed and the M- and L-cones are randomly distributed.

    Throughout the whole retina the ratio of L- and M- cones to S-cones is about 100:1.

    Spatial Acuity Estimate From Mosaic

    From the cone mosaic we can estimate spatial acuity or the ability to see fine detail.

    In the central fovea, there are approximately 150,000 cones/ sq. mm. The distance between cone centers in the hexagonal packing of the cones is about 0.003 mm. To convert this to degrees of visual angle you need to know that there are 0.29 mm/deg so that the spacing is 0.003/0.29 = 0.013° between cone centers.

    The Nyquist frequency, f, is the frequency at which aliasing begins. That is a grating pattern of cos(2*pi(N/2+f)) above the Nyquist frequency is indistinguishable from the signal cos(2*pi(N/2-f)) below the Nyquist frequency where N is the number of sample points per unit distance. The Nyquist frequency is f = 1/N. The value of N = 1/0.0102 = 97. Therefore f = 48 cycles per degree.

    In actuality, the foveal Nyquist limit is more like 60 cycles per degree. This may be a result of the hexagonal rather than the rectangular packing of the cone mosaic. The optics of the eye blur the retinal image so that this aliasing is not produced. Using laser interferometry, the optics of the eye can be bypassed so we can reveal this aliasing. We will discuss this in more detail in the chapter on visual acuity.

    The mosaic of the retina in addition to the processing in the visual system produces another ability to see fine resolution and ascertain alignment of object called hyperacuity . People have the ability to see misalignment of objects of 5 seconds of arc (which is 1/5 of a cone width). This corresponds to seeing the misalignment in headlights 39 miles away. Maybe you can try working this out to see if I am exaggerating.


    Are all cone cells connected directly to the brain? - Biology

    There are two types of photoreceptors in the human retina, rods and cones .

    Rods are responsible for vision at low light levels ( scotopic vision ). They do not mediate color vision, and have a low spatial acuity.

    Cones are active at higher light levels ( photopic vision ), are capable of color vision and are responsible for high spatial acuity. The central fovea is populated exclusively by cones. There are 3 types of cones which we will refer to as the short-wavelength sensitive cones, the middle-wavelength sensitive cones and the long-wavelength sensitive cones or S-cone, M-cones, and L-cones for short.

    The light levels where both are operational are called mesopic .

    The bottom figure shows the distribution of rods and cones in the retina. This data was prepared from histological sections made on human eyes.

    In the top figure, you can relate visual angle to the position on the retina in the eye.

    Notice that the fovea is rod-free and has a very high density of cones. The density of cones falls of rapidly to a constant level at about 10-15 degrees from the fovea. Notice the blind spot which has no receptors.

    At about 15°-20° from the fovea, the density of the rods reaches a maximum. (Remember where Hecht, Schlaer, and Pirenne presented their stimuli.) A longitudinal section would appear similar however there would be no blind spot. Remember this if you want to present peripheral stimuli and you want to avoid the blind spot.

    Here is a figure from the textbook that shows the changes in the size of the photoreceptors with eccentricity. The bottom graph shows individual variations in the density of cones.

    Here are schematic diagrams of the structure of the rods and cones:

    This figure shows the variety in the shapes and sizes of receptors across and within species.

    Here is a summary of the properties and the differences in properties between the rods and cones:

    If you look above at the schematic diagram of the rods and cones, you will see that in the outer segments of rods the cell membrane folds in and creates disks. In the cones, the folds remain making multiple layers. The photopigment molecules reside in membranes of these disks and folds. They are embedded in the membranes as shown in the diagram below where the two horizontal lines represent a rod disk membrane (either the membrane on the top or bottom of the disk) and the circles represent the chain of amino acids that make up a rhodopsin molecule. Rhodopsin is the photopigment in rods.

    Each amino acid, and the sequence of amino acids are encoded in the DNA. Each person possesses 23 pairs of chromosomes that encode the formation of proteins in sequences of DNA. The sequence for a particular protein is called a gene. In recent years, researchers have identified the location and chemical sequence of the genes that encode the photopigments in the rods and cones.

    This figure shows the structure of the rhodopsin molecule. The molecule forms 7 columns that are embedded in the disk membrane. Although not shown in this schematic, the columns are arranged in a circle like the planks of a barrel. (Another molecule called a chromophore binds within this barrel.)

    Each circle is an amino-acid which are the building blocks of proteins. Each amino acid is encoded by a sequence of three nucleic acids in the DNA.

    Before identifying the genetic sequence of human rhodopsin, it was sequences in other animals. Here is shown the comparison between the bovine (cow) sequence and the human sequence. They are very similar with only a small number of differences (the dark circles). Even when there is a difference it may not be functionally significant.

    The gene for human rhodopsin is located on chromosome 3.

    This figure shows the sequence for the S-cone pigment compared to that of rhodopsin. The S-cone pigment gene is located on chromosome 7. Notice how different they are.

    This figure shows the sequence of the L- and M-cone pigments compared to each other. These pigments are very similar. Only those differences within the cell membrane can contribute to the differences in their spectral sensitivity.

    The M- and L- cone pigments are both encoded on the X chromosome in tandem. The 23rd pair of chromosomes determines gender. For females this pair is XX and for males this pair is XY.

    We will return to this later on when we discuss color vision and color blindness.

    This figure shows how the three cone types are arranged in the fovea. Currently there is a great deal of research involving the determination of the ratios of cone types and their arrangement in the retina.

    This diagram was produced based on histological sections from a human eye to determine the density of the cones. The diagram represents an area of about 1° of visual angle. The number of S-cones was set to 7% based on estimates from previous studies. The L-cone:M-cone ratio was set to 1.5. This is a reasonable number considering that recent studies have shown wide ranges of cone ratios in people with normal color vision. In the central fovea an area of approximately 0.34° is S-cone free. The S-cones are semi-regularly distributed and the M- and L-cones are randomly distributed.

    Throughout the whole retina the ratio of L- and M- cones to S-cones is about 100:1.

    Spatial Acuity Estimate From Mosaic

    From the cone mosaic we can estimate spatial acuity or the ability to see fine detail.

    In the central fovea, there are approximately 150,000 cones/ sq. mm. The distance between cone centers in the hexagonal packing of the cones is about 0.003 mm. To convert this to degrees of visual angle you need to know that there are 0.29 mm/deg so that the spacing is 0.003/0.29 = 0.013° between cone centers.

    The Nyquist frequency, f, is the frequency at which aliasing begins. That is a grating pattern of cos(2*pi(N/2+f)) above the Nyquist frequency is indistinguishable from the signal cos(2*pi(N/2-f)) below the Nyquist frequency where N is the number of sample points per unit distance. The Nyquist frequency is f = 1/N. The value of N = 1/0.0102 = 97. Therefore f = 48 cycles per degree.

    In actuality, the foveal Nyquist limit is more like 60 cycles per degree. This may be a result of the hexagonal rather than the rectangular packing of the cone mosaic. The optics of the eye blur the retinal image so that this aliasing is not produced. Using laser interferometry, the optics of the eye can be bypassed so we can reveal this aliasing. We will discuss this in more detail in the chapter on visual acuity.

    The mosaic of the retina in addition to the processing in the visual system produces another ability to see fine resolution and ascertain alignment of object called hyperacuity . People have the ability to see misalignment of objects of 5 seconds of arc (which is 1/5 of a cone width). This corresponds to seeing the misalignment in headlights 39 miles away. Maybe you can try working this out to see if I am exaggerating.


    Are all cone cells connected directly to the brain? - Biology

    Homeostasis: the maintenance of a constant internal environment.

    All organisms try and maintain a constant internal environment. This is called homeostasis. Examples of homeostasis include the regulation of water levels (see above) and the regulation of body temperature (see below).

    Humans have two systems which carry out homeostasis

    Nervous System – immediate responses to stimuli (sec - hours)
    Endocrine System – long term responses to stimuli (hours - months)

    Both systems respond to stimuli (i.e. events that change the internal environment). Both systems have a detector (which detects the stimulus) and an effector, which carries out a response to correct the effect of the stimulus. The message from detector to effector is carried either via an electrical nerve impulse or as a hormone, depending which homeostatic system is being used.

    Coordination in Humans:

    Nerves & the Nervous system:

    The nervous system consists of the brain and the spinal cord.
    Sense organs (e.g. pain receptors in skin, or photoreceptors in the eye) are linked to the brain via nerves.
    Stimulation of the sense organs results in an electrical signal (a nerve impulse) being sent along the nerve to the brain. Nerve impulses are very quick (

    120m/s), allowing rapid responses to the stimulus. Some sense organs are not connected directly to the brain. This is a defense mechanism allowing almost instant responses to threatening or dangerous stimuli (e.g. pain). These instant responses are controlled by nerves in the spine, rather than the brain and are called reflexes

    1. A stimulus is detected by a receptor
    2. The receptor initiates a nerve impulse in the sensory nerve
    3. The sensory nerve (which runs from the receptor to the spine) passes the message onto an interneurone in the spine
    4. The interneurone passes the message on the a motor nerve
    5. The motor nerve (which runs from the spine to a muscle in the same limb as the receptor) passes the message onto the effector muscle
    6. The effector muscle carries out the response.

    The entire process (stimulus to response) happens in less than a second and does not involve the brain. The purpose of the interneurone is to inform the brain of what has happened.

    Cornea - Refracts (bends) light entering the eye.
    Iris - Controls the amount of light entering the eye by adjusting the size of the pupil.
    Pupil - Hole which allows light into the eye.
    Lens - Allows fine focusing by changing shape.
    Ciliary muscle - Changes the shape of the lens by altering the tension on the suspensory ligaments.
    Retina - Contains light-sensitive rod and cone cells which convert light energy into a nerve impulse (i.e. transduce energy).
    Fovea - Area where most light is focused, very sensitive to colour (most cones here).
    Optic nerve - Transmits nerve impulses to the brain, where they are interpreted.
    Sclera - Outer protective layer of eye
    Choroid - Contains blood vessels

    Light is detected by photoreceptors in the eye. These receptors form the retina (the inner lining of the eye). There are two types of photoreceptor

    - Rods, which see only in black & white
    - Cones, which see in either red, blue or green (3 types of cone)

    There are two types of reflex you need to know about in the eye

    1. Responding to different light levels
    2. Focusing the eye

    Responding to different light levels:

    1. Photoreceptors detect
    2. Reflex occurs
    3. Muscles in the Iris are the effectors
    - Radial muscles in Iris contract
    - Circulatory muscles in Iris relax
    4. Pupil diameter opens
    5. More light enters the eye

    1. Photoreceptors detect
    2. Reflex occurs
    3. Muscles in the Iris are the effectors
    - Radial muscles in Iris relax
    - Circulatory muscles in Iris contract
    4. Pupil diameter closes
    5. Less light enters the eye

    Near Object
    1. Incoming light is divergent
    2. Ciliary muscles contract
    3. Suspensory ligaments are loose
    4. Lens becomes fat
    5. Light is refracted more
    Light converges on the retina

    Distant Object
    1. Incoming light is parallel
    2. Ciliary muscles relax
    3. Suspensory ligaments are tight
    4. Lens is pulled thin
    5. Light is refracted less
    Light converges on the retina

    Controlling Skin temperature:

    Too hot
    When you are hot the following happen (controlled by reflexes)
    1. Hairs on skin lie flat (less insulating air trapped)
    2. Sweating starts
    3. Blood is diverted close to the surface of the skin (more heat radiation)

    Too cold
    When you are cold the following happen (controlled by reflexes)
    1. Hairs on skin stand up (more insulating air trapped)
    2. Sweating stops
    3. Shivering starts, so muscles respire more, producing more heat
    4. Blood is diverted away from the surface of the skin (less heat radiation)

    Arterioles in the skin can open and close in response to nerve messages.

    Vasoconstriction – arteriole closes
    Vasodilation – arteriole opens

    The net effect is to open arterioles under the surface of the skin when hot and close them when cold.

    Random Hormones you need to know:

    It might be worth your while looking these up in more detail…

    1. You eat a meal. It is digested and glucose is absorbed into the blood stream.
    2. Blood glucose level rises
    3. Pancreas detects
    4. Pancreas releases insulin into bloodstream
    5. Insulin travels all over the body
    6. Only the cells in the liver have receptors for insulin, so only they respond to the hormone.
    7. The liver cells (they’re called hepatocytes) take up the glucose out of the blood stream.
    8. The glucose if converted into glycogen, which is stored inside liver cells.
    9. Blood glucose level falls back to normal.

    The hormone glucagon does exactly the opposite to insulin. Glucagon is released when blood glucose levels fall too low.

    Hyperglycaemia: blood glucose level is dangerously high (causes coma and can be fatal)
    Hypoglycaemia: blood glucose level is dangerously high (causes coma and can be fatal)


    Chapter 15 The Special Senses (TB)

    What structure regulates the amount of light passing to the visual receptors of the eye?

    A) iris
    B) cornea
    C) aqueous humor
    D) lens

    Receptors for hearing are located in the ________.

    A) semicircular canals
    B) cochlea
    C) vestibule
    D) tympanic membrane

    Which of the follow types of neurons are replaced throughout adult life?

    A) olfactory receptor cells
    B) retinal ganglion cells
    C) auditory outer and inner hair cells
    D) retinal bipolar cells

    The oil component found in tears is produced by the ________.

    A) tarsal glands
    B) ciliary gland
    C) lacrimal glands
    D) conjunctiva

    The receptor for static equilibrium is the ________.

    A) cochlear duct
    B) macula
    C) utricle
    D) semicircular canals

    Farsightedness is more properly called ________.

    A) hyperopia
    B) presbyopia
    C) hypopia
    D) myopia

    Seventy percent of all sensory receptors are located in the ________.

    A) eye
    B) skin
    C) ears
    D) nose

    Which of the following structures is not part of the external ear?

    A) pharyngotympanic tube
    B) tympanic membrane
    C) external acoustic meatus
    D) pinna

    Nerve fibers from the medial aspect of each eye ________.

    A) go to the superior colliculus only
    B) divide at the chiasma, with some crossing and some not crossing
    C) cross over to the opposite side at the chiasma
    D) pass posteriorly without crossing over at the chiasma

    Ordinarily, it is not possible to transplant tissues from one person to another, yet corneas canbe transplanted without tissue rejection. This is because the cornea ________.

    A) is not a living tissue
    B) does not contain connective tissue
    C) has no blood supply
    D) has no nerve supply

    The oval window is connected directly to which passageway?

    A) external acoustic meatus
    B) scala tympani
    C) pharyngotympanic tube
    D) scala vestibuli

    There are three layers of neurons in the retina. The axons of which of these neuron layersform the optic nerves?

    A) bipolar cells
    B) ganglion cells
    C) cone cells
    D) rod cells

    The first "way station" in the visual pathway from the eye, after there has been partialcrossover of the fibers in the optic chiasma, is the ________.

    A) visual cortex
    B) superior colliculi
    C) lateral geniculate body of the thalamus
    D) temporal lobe

    As sound levels increase in the spiral organ (of Corti), ________.

    A) outer hair cells stiffen the basilar membrane
    B) outer hair cells bend the cilia away from the kinocilium
    C) inner hair cells bend the cilia away from the kinocilium
    D) inner hair cells stiffen the basilar membrane

    Which of the following is true about gustatory receptors?

    A) The receptors generate an action potential in response to chemical stimuli.
    B) Complete adaptation occurs in about one to five minutes.
    C) In order for a chemical to be sensed, it must be hydrophobic.
    D) All gustatory receptors have the same threshold for activation.

    Taste buds are not found ________.

    A) in filiform papillae
    B) in circumvallate papillae
    C) in fungiform papillae
    D) lining the buccal cavity

    Select the correct statement about olfaction.

    A) Substances must be volatile and hydrophobic in order to activate olfactory receptors.
    B) Olfactory adaptation is only due to fading of receptor cell response.
    C) Some of the sensation of olfaction is actually one of pain.
    D) Olfactory receptors have a high degree of specificity toward a single type of chemical.

    What prevents the eyelids from sticking together when the eyes close?

    A) tarsal gland secretions
    B) conjunctival fluid
    C) ciliary gland secretions
    D) lacrimal fluid

    Which of the following taste sensations is incorrectly matched to the chemicals that produceit?

    A) bitteralkaloids
    B) souracids
    C) saltymetal ions
    D) sweetorganic substances such as sugar and some lead salts
    E) umamiamino acids glutamate and lysine

    U.S. employees must wear hearing protection at ________ dB or above.

    A) bone in the center of a semicircular canal
    B) a bony area around the junction of the facial, vestibular, and cochlear nerves
    C) bone around the cochlea
    D) a bone pillar in the center of the cochlea

    Which statement about malnutrition-induced night blindness is most accurate?

    A) The most common cause is vitamin D deficiency.
    B) Vitamin supplements can reverse degenerative changes.
    C) Visual pigment content is reduced in both rods and cones.
    D) The impaired vision is caused by reduced cone function.

    A) involves accumulation of rhodopsin
    B) is much faster than light adaptation
    C) involves improvement of acuity and color vision
    D) results in inhibition of rod function

    Conscious perception of vision probably reflects activity in the ________.

    A) thalamus
    B) superior colliculus
    C) occipital lobe of the cortex
    D) chiasma

    In the visual pathways to the brain, the optic radiations project to the ________.

    A) medial retina
    B) optic chiasma
    C) lateral geniculate body
    D) primary visual cortex

    Visual inputs to the ________ serve to synchronize biorhythms with natural light and dark.

    A) superior colliculi
    B) lateral geniculate body
    C) pretectal nuclei
    D) suprachiasmatic nucleus

    Information from balance receptors goes directly to the ________.

    A) back muscles
    B) visual cortex
    C) brain stem reflex centers
    D) motor cortex

    Motion sickness seems to ________.

    A) respond best to medication that "boosts" vestibular inputs
    B) respond best to medication taken after salivation and pallor begins
    C) result from activation of nausea centers in the brain stem
    D) result from mismatch between visual and vestibular inputs

    A) the fetus cannot see and therefore visual cortical connections are not made
    B) the fetus can see only light and shadow, but not forms, so partial visual connections are made
    C) scanty visual connections are made that proliferate greatly during infancy
    D) despite the fact that the fetus cannot see, functional visual cortical connections are established

    A) cry with copious tears
    B) often use only one eye at a time
    C) see in tones of red and green only
    D) are myopic

    The blind spot of the eye is where ________.

    A) the macula lutea is located
    B) only cones occur
    C) the optic nerve leaves the eye
    D) more rods than cones are found

    The first vestiges of eyes in the embryo are called ________.

    A) mesenchyme
    B) optic cups
    C) optic vesicles
    D) optic discs

    Which pairing of terms is incorrectly related?

    A) amplitude: sound intensity
    B) frequency: wavelength number
    C) frequency: loudness
    D) quality: frequency number

    Olfactory cells and taste buds are normally stimulated by ________.

    A) substances in solution
    B) movement of a cupula
    C) stretching of the receptor cells
    D) the movement of otoliths

    Which of the following could not be seen as one looks into the eye with an ophthalmoscope?

    A) fovea centralis
    B) macula lutea
    C) optic disc
    D) optic chiasma

    The cells of the retina in which action potentials are generated are the ________.

    A) ganglion cells
    B) bipolar cells
    C) amacrine cells
    D) rods and cones

    During dark adaptation ________.

    A) the rate of rhodopsin breakdown is accelerated
    B) the sensitivity of the retina decreases
    C) the cones are activated
    D) rhodopsin accumulates in the rods

    Tinnitis, vertigo, and gradual hearing loss typify the disorder called ________.

    A) Ménière's syndrome
    B) conjunctivitis
    C) motion sickness
    D) strabismus

    Which of the following is not a characteristic of olfactory receptor cells?

    A) They have a short life span of about 60 days.
    B) They are unipolar neurons.
    C) They are ciliated.
    D) They are chemoreceptors.

    An essential part of the maculae involved in static equilibrium is (are) the ________.

    A) otoliths
    B) cupula
    C) spiral organ (of Corti)
    D) scala media

    Which of the following is true about light and vision?

    A) Light is a form of electromagnetic radiation that slows down as it enters a medium ofrelatively less density.
    B) The greater the incident angle of light striking a refractive surface, the less the amount of lightbending.
    C) When we see the color of an object, all light is being absorbed by that object except for thecolor being experienced.
    D) Human photoreceptors respond to light in the 100-300 nm range.

    The tarsal plate of the eyelid ________.

    A) is connected to the superior rectus muscle
    B) is composed of connective tissue surrounding a thin cartilage plate
    C) is connected to the levator palpebrae
    D) assists in the act of winking

    Which of the following is true about photoreceptors?

    A) Three types of color-sensitive photoreceptors exist: red, green, and yellow.
    B) If all cones are stimulated equally, all colors are absorbed by the cones and the colorperceived is black.
    C) In dim light, images are focused directly on the rods in the fovea centralis.
    D) Rods absorb light throughout the visual spectrum but confer only gray tone vision.

    The eye muscle that elevates and turns the eye laterally is the ________.

    A) lateral rectus
    B) medial rectus
    C) superior oblique
    D) inferior oblique

    The receptor membranes of gustatory cells are ________.

    A) fungiform papillae
    B) basal cells
    C) taste buds
    D) gustatory hairs

    Light passes through the following structures in which order?

    A) vitreous humor, lens, aqueous humor, cornea
    B) cornea, vitreous humor, lens, aqueous humor
    C) cornea, aqueous humor, lens, vitreous humor
    D) aqueous humor, cornea, lens, vitreous humor

    Damage to the medial recti muscles would probably affect ________.

    A) convergence
    B) accommodation
    C) refraction
    D) pupil constriction

    Which statement about sound localization is not true?

    A) It uses time differences between sound reaching the two ears.
    B) It requires processing at the cortical level.
    C) It is difficult to discriminate sound sources in the midline.
    D) It requires input from both ears.

    Which of the following is not a possible cause of conduction deafness?

    A) middle ear infection
    B) otosclerosis
    C) impacted cerumen
    D) cochlear nerve degeneration

    Visual processing in the thalamus does not contribute significantly to ________.

    A) movement perception
    B) high-acuity vision
    C) depth perception
    D) night vision

    Visible light fits between ________.

    A) UV and infrared
    B) microwaves and radio waves
    C) X rays and UV
    D) gamma rays and infrared

    Ceruminous glands are ________.

    A) saliva glands found at the base of the tongue
    B) glands found in the lateral corners of your eye
    C) modified apocrine sweat glands
    D) modified taste buds

    Presbyopia is not ________.

    A) the unequal curvature of refracting surfaces
    B) called ʺold personʹs visionʺ
    C) the loss of elasticity of the lens
    D) common in individuals over 50

    Inhibitory cells in the olfactory bulbs are called _________.

    A) sustentacular cells
    B) mitral cells
    C) granule cells
    D) basal cells

    There are three layers of neurons in the retina. The axons of which of these neuron layers form the optic nerves?

    A) cone cells
    B) bipolar cells
    C) ganglion cells
    D) rod cells

    A) possess an inner segment, which is the receptor region
    B) replicate to replace damaged cells, in order to maintain normal vision
    C) package visual pigment in membrane-bound discs, which increases the efficiency of light trapping
    D) called cones possess a short conical inner segment

    Olfactory glands function to ________.

    A) secrete mucus
    B) produce olfactory cells
    C) assist in detection of odors
    D) produce Ca+ ions that are taken up by the olfactory receptor cells for their use

    The ciliary body does not ________.

    A) attach to the iris
    B) belong to the anterior chamber of the eye
    C) pull on the ciliary zonule
    D) secrete aqueous humor

    As sound intensity increases, we hear the sound as a louder sound at the same pitch. This suggests that ________.

    A) 540-Hz-receptive cells are particularly refractory
    B) inhibitory postsynaptic potentials (IPSPs) are building up in the auditory cortex
    C) cochlear cells that respond to the same pitch vary in responsiveness
    D) the timing of the cochlear vibrations encodes the pitch

    ________ is a disorder of the olfactory nerves.

    A) Anosmias
    B) Uncinate fits
    C) Scotoma
    D) Otalgia

    What part of the eye is called "the white of the eye"?

    A) the sclera
    B) the choroid

    In which layer is the retina found?

    Which iris color has more melanin?

    Which iris color has more melanin?

    What are the protein fibers called that make up the lens?

    A) collagens
    B) crystallins

    What do we call the gel-like substance in the posterior chamber of the eyeball?


    Watch the video: ABC Zoom - Colour vision: cone cells, retinal and light (May 2022).